Most human melanomas of the superficial spreading and nodular clinical subtypes contain activating mutations in either the NRAS small GTPase or the BRAF protein kinase. To determine the possible functional consequences of the molecular heterogeneity of human melanomas, we have begun to characterize the set of signalling pathways stimulated by RAS in both categories of human melanomas. We hypothesize that NRAS melanomas may exhibit activation of additional, RAS-dependent signalling pathways than BRAF melanomas. As such, alternative RAS-dependent signalling pathways may be relevant as molecular targets for human melanoma, at least for that class of human melanomas exhibiting activating mutations in NRAS.